ライフサイエンスコーパス: lapatinib

1 to dampen sensitivity of the cancer cells to lapatinib.

2 diate resistance to the ERBB2-targeted agent lapatinib.

3 who have previously received trastuzumab and lapatinib.

4 diarrhea, fatigue, and rash associated with lapatinib.

5 iants in 1,194 patients randomly assigned to lapatinib.

6 in C, doxorubicin, cisplatin, sorafenib, and lapatinib.

7 served more frequently in patients receiving lapatinib.

8 regulin (P = 0.026) predicted sensitivity to lapatinib.

9 , which were then exposed to trastuzumab and lapatinib.

10 sponse to the HER2 tyrosine kinase inhibitor lapatinib.

11 with chemotherapy plus either trastuzumab or lapatinib.

12 between the direct effects of cetuximab and lapatinib.

13 tched to erlotinib, gefitinib, afatinib, and lapatinib.

14 d ErbB3, that is disrupted by treatment with lapatinib.

15 g P-Akt and limiting the antitumor action of lapatinib.

16 gulated in primary HER2+ tumors treated with lapatinib.

17 gistically enhances the apoptotic effects of lapatinib.

18 ponses to the HER2-targeted kinase inhibitor lapatinib.

19 the pro-apoptotic effects of trastuzumab and lapatinib.

20 ity of the cancer cells to a HER2 inhibitor, lapatinib.

21 in arm C, patients received trastuzumab and lapatinib 1,000 mg PO daily.

22 ned (1:1) to receive lapatinib-capecitabine (lapatinib 1,250 mg per day; capecitabine 2,000 mg/m(2) p

23 28 and every 4 weeks thereafter, and either lapatinib 1,500 mg or placebo daily.

24 d by 2 mg weekly; in arm B patients received lapatinib 1,500 mg orally (PO) daily; and in arm C, pati

25 months of letrozole 2.5 mg orally daily plus lapatinib 1,500 mg orally daily or placebo.

26 ence in PFS (hazard ratio [HR] of placebo to lapatinib, 1.04; 95% CI, 0.82 to 1.33; P = .37); median

27 per week (4 mg/kg loading, then 2 mg/kg) and lapatinib 1000 mg once per day for 12 weeks.

28 mg/kg loading dose followed by 2 mg/kg), or lapatinib (1000 mg) plus trastuzumab (same dose as for s

29 OR CORRECTED], subsequent doses 2 mg/kg), or lapatinib (1000 mg) plus trastuzumab.

30 aily on days 1-14 on each 21-day cycle, plus lapatinib 1250 mg orally once daily on days 1-21).

31 2 mg/kg intravenously) weekly until surgery, lapatinib (1250 mg orally) daily until surgery, or weekl

32 nts occurred in 149 (99%) patients receiving lapatinib, 142 (96%) patients receiving trastuzumab, and

33 FINDINGS: 154 patients received lapatinib, 149 trastuzumab, and 152 the combination.

34 s with EGFR-positive CTCs were recruited and lapatinib 1500 mg daily was administered, in a standard

35 ere randomly assigned (1:1) to receive daily lapatinib (1500 mg) or daily placebo for 12 months.

36 r and randomly assigned them to receive oral lapatinib (1500 mg), intravenous trastuzumab (4 mg/kg lo

37 m in diameter were randomly assigned to oral lapatinib (1500 mg), intravenous trastuzumab (loading do

38 r-enzyme alterations were more frequent with lapatinib (27 [17.5%]) and lapatinib plus trastuzumab (1

39 equency of grade 3 diarrhoea was higher with lapatinib (36 patients [23.4%]) and lapatinib plus trast

40 no significant difference in pCR between the lapatinib (38 of 154 patients [24.7%, 18.1-32.3]) and th

41 (488 patients treated with capecitabine plus lapatinib, 490 patients treated with trastuzumab emtansi

42 ly until surgery, or weekly trastuzumab plus lapatinib (750 mg orally) daily until surgery.

43 overall survival was 93% (95% CI 87-96) for lapatinib, 90% (84-94) for trastuzumab, and 95% (90-98)

44 , TBK1/IKKepsilon inhibition cooperated with lapatinib, a HER2/EGFR1-targeted drug, to accelerate apo

45 mab, and following subsequent treatment with lapatinib, a splicing mutation in GAS6 (growth arrest-sp

46 trastuzumab (TZ), a monoclonal antibody, and lapatinib, a tyrosine kinase inhibitor, have proved high

47 TZ and lapatinib ability to block extracellular signal-regulate

48 ib and the FDA-approved ErbB1/2-directed TKI lapatinib abrogated proliferation and increased sensitiv

49 tivation using the tyrosine kinase inhibitor lapatinib abrogates the effects of BTG2 knockdown, inclu

50 HER2 blockade consisting of trastuzumab and lapatinib added to paclitaxel, considering tumor and mic

51 previously treated with both trastuzumab and lapatinib (advanced setting) and a taxane (any setting)

52 Further, lapatinib, AEE788, and canertinib were docked to TbLBPKs

53 Purpose To establish whether maintenance lapatinib after first-line chemotherapy is beneficial in

54 fectiveness of the tyrosine kinase inhibitor lapatinib against HER2 gene-amplified breast cancers, mo

55 rc inhibitor AZD0530 was more effective than lapatinib alone at inhibiting pAkt and growth of establi

56 us trastuzumab improves outcomes relative to lapatinib alone in heavily pretreated, human epidermal g

57 se-dependent, and inhibited by erlotinib and lapatinib, although to differing extents.

58 were randomized to letrozole with or without lapatinib, an epidermal growth factor receptor (EGFR)/HE

59 rmore, ErbB2-directed RNAi or treatment with lapatinib, an ErbB2/EGFR small-molecule inhibitor used f

60 Lapatinib, an inhibitor of HER2 and EGFR, was more effec

61 bined with the EGFR/HER2 dual-targeting drug lapatinib, an Src-targeting combinatorial regimen preven

62 adverse events were similar in both arms (6% lapatinib and 5% placebo).

63 e response) were observed (70% for letrozole-lapatinib and 63% for letrozole-placebo).

64 occurred in 99 (6%) of 1573 patients taking lapatinib and 77 (5%) of 1574 patients taking placebo, w

65 Lapatinib and CBL0137 synergistically inhibited the prol

66 Lapatinib and imatinib may cause clinically significant

67 Lapatinib and indirubin-3'-monoxime showed moderate hCOX

68 r-positive/HER2-negative patients, letrozole-lapatinib and letrozole-placebo resulted in a similar ov

69 del is used to quantify two different drugs, lapatinib and nevirapine, in dosed tissues from nonclini

70 udies in breast cancer cells have shown that lapatinib and obatoclax interact in a greater than addit

71 Previous studies showed that lapatinib and obatoclax interact in a greater-than-addit

72 Lapatinib and obatoclax killed multiple CNS tumor isolat

73 Lapatinib and obatoclax killed multiple tumor cell types

74 Altogether, our data show that lapatinib and obatoclax therapy could be of use in the t

75 cient rho-zero cells were radiosensitized by lapatinib and obatoclax treatment.

76 n plays an essential role in cell killing by lapatinib and obatoclax, as well as radiosensitization b

77 Taken together, our data argue that lapatinib and obatoclax-induced toxic autophagy is due t

78 Lapatinib and obatoclax-initiated autophagy depended on

79 Importantly, lapatinib and palbociclib strictly block de novo synthes

80 Combined lapatinib and panobinostat treatment interacted synergis

81 The overall survival for lapatinib and placebo was 12.6 (95% CI, 9.0 to 16.2) and

82 The median PFS for lapatinib and placebo was 4.5 (95% CI, 2.8 to 5.4) and 5

83 The rate of grade 3 to 4 adverse events for lapatinib and placebo was 8.6% versus 8.1% ( P = .82).

84 sine kinase inhibitors, including erlotinib, lapatinib and sunitinib.

85 toma cells between the EGFR kinase inhibitor lapatinib and the anticancer compound YM155 that is pres

86 Finally, the combination of lapatinib and the Src inhibitor AZD0530 was more effecti

87 was significantly higher in the group given lapatinib and trastuzumab (78 of 152 patients [51.3%; 95

88 icant 4.5-month median OS advantage with the lapatinib and trastuzumab combination and support dual H

89 hosphamide treatment, and of the addition of lapatinib and trastuzumab combined after doxorubicin plu

90 val did not significantly differ between the lapatinib and trastuzumab groups (HR 0.86, 95% CI 0.45-1

91 ent-free survival did not differ between the lapatinib and trastuzumab groups (HR 1.06, 95% CI 0.66-1

92 Early use of lapatinib and trastuzumab is active in human epidermal g

93 breast cancer showed that the combination of lapatinib and trastuzumab significantly improved rates o

94 mice by inhibition of the HER2 pathway with lapatinib and trastuzumab to block all homo- and heterod

95 ere consistent with known safety profiles of lapatinib and trastuzumab.

96 and 2B17) by four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using he

97 Neo-ALTTO (Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimisation) enr

98 ancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization tria

99 The NeoALTTO trial (Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization) ran

100 attributed to flucloxacillin, ximelagatran, lapatinib, and amoxicillin-clavulanate.

101 nts such as gefitinib, erlotinib, cetuximab, lapatinib, and panitumumab have less systemic side-effec

102 advanced setting, including trastuzumab and lapatinib, and previous taxane therapy in any setting, w

103 The 4-anilinoquinazolines canertinib and lapatinib, and the pyrrolopyrimidine AEE788 killed blood

104 carrying orthotopic CNS tumor isolates with lapatinib- and obatoclax-prolonged survival.

105 sed (trastuzumab) vs a small molecule-based (lapatinib) anti-HER2 therapy.

106 The increase in ALT case incidence in the lapatinib arm showed no evidence of plateau during 1 yea

107 In the letrozole-lapatinib arm, the probability of achieving a clinical r

108 HER2-directed drugs such as trastuzumab and lapatinib as well as depletion of HER2 or HER3 stimulate

109 showing a trend of increasing sensitivity to lapatinib as YAP decreased.

110 osphorylation was reduced by ErbB2 inhibitor lapatinib, as well as by knockdown of PKC-delta but not

111 ells, both sensitive and resistant to TZ and lapatinib, as well as in a preclinical BC model resistan

112 blasts strongly protect carcinoma cells from lapatinib, attributable to its reduced accumulation in c

113 inib bound to Tb927.4.5180 (termed T. brucei lapatinib-binding protein kinase-1 (TbLBPK1)) while AEE7

114 Lapatinib binds to a unique conformation of protein kina

115 lapatinib exposure, despite highly variable lapatinib bioavailability.

116 on sensitizes HER2(+) breast cancer cells to lapatinib both in vitro and in vivo, including JAK2/STAT

117 HER2+ breast cancer cells and xenografts to lapatinib both in vitro and in vivo.

118 Lapatinib bound to Tb927.4.5180 (termed T. brucei lapati

119 longer with trastuzumab-capecitabine versus lapatinib-capecitabine (hazard ratio [HR] for PFS, 1.30;

120 ases were randomly assigned (1:1) to receive lapatinib-capecitabine (lapatinib 1,250 mg per day; cape

121 f relapse was 3% (eight of 251 patients) for lapatinib-capecitabine and 5% (12 of 250 patients) for t

122 17% (45 of 267 patients) of patients in the lapatinib-capecitabine and trastuzumab-capecitabine arms

123 However, lapatinib-capecitabine efficacy may have been affected b

124 -positive metastatic breast cancer receiving lapatinib-capecitabine or trastuzumab-capecitabine.

125 rly with 540 enrolled patients (271 received lapatinib-capecitabine, and 269 received trastuzumab-cap

126 ieved with chemotherapy plus trastuzumab and lapatinib compared with chemotherapy plus either trastuz

127 edictive effect on risk for progression with lapatinib compared with trastuzumab among patients with

128 exes, which confirmed that TbLBPKs can adopt lapatinib-compatible conformations.

129 c responses were seen in three patients with lapatinib concentrations approaching 10,000 ng/mL.

130 e-daily dosing with no DLTs; however, plasma lapatinib concentrations plateaued in this dose range.

131 2 values (HR per 10-ng/mL increase in sHER2: lapatinib-containing therapies, 1.009 v nonlapatinib-con

132 benefit (HR per 10-ng/mL increase in sHER2: lapatinib-containing therapies, 1.017 v nonlapatinib-con

133 33 [48%] of 490) than with capecitabine plus lapatinib control treatment (291 [60%] of 488).

134 uzumab emtansine (n=495) or capecitabine and lapatinib (control; n=496).

135 atients, the HER2 inhibitors trastuzumab and lapatinib controlled tumor progression in the breast but

136 ted that resistance to the ERBB1/2 inhibitor lapatinib could be overcome by the B cell CLL/lymphoma-2

137 Similarly, inhibition of ErbB RTKs with lapatinib did not affect PI3K signaling in PIK3CA(H1047R

138 ule tyrosine kinase inhibitors erlotinib and lapatinib differentially enhance the dimerization of the

139 Lapatinib dose was escalated to 7,000 mg per day in twic

140 ERBB2 Mab), pertuzumab (anti-ERBB2 Mab), and lapatinib (dual ERBB1 and ERBB2 tyrosine kinase inhibito

141 Trastuzumab and lapatinib each synergized with XL147 for inhibition of p

142 In addition, both canertinib and lapatinib eluted Tb10.60.3140 (TbLBPK4), whereas only ca

143 ed from the protocol, AEE788, canertinib and lapatinib eluted TbLBPK1, TbLBPK2, and Tb927.3.1570 (TbL

144 ment with the HER2 inhibitors trastuzumab or lapatinib enhanced XL147-induced cell death and inhibiti

145 Lapatinib exhibited potent competitive inhibition agains

146 Lapatinib exposure can be safely and significantly incre

147 hese, only ketoconazole was able to increase lapatinib exposure, despite highly variable lapatinib bi

148 nal cohorts evaluated strategies to increase lapatinib exposure, including the food effect, CYP3A4 in

149 ; MK2206 for PIK3CA, AKT, or PTEN mutations; lapatinib for ERBB2 mutations or amplifications; and sun

150 stigated the efficacy and safety of adjuvant lapatinib for patients with trastuzumab-naive HER2-posit

151 Substitution of lapatinib for trastuzumab in combination with chemothera

152 o neoadjuvant therapy of the substitution of lapatinib for trastuzumab in combination with weekly pac

153 ively by the small-molecule kinase inhibitor lapatinib frequently acquire resistance to this drug.

154 as powered for a 50% improvement in PFS with lapatinib from 5 to 7.5 months.

155 91 (53.2%, 45.4-60.3) of 171 patients in the lapatinib group (p=0.9852); and 106 (62.0%, 54.3-68.8) o

156 ade 4 in five patients (3%), 28 [16%] in the lapatinib group [grade 4 in eight patients (5%)], and 29

157 ow-up of 47.4 months (range 0.4-60.0) in the lapatinib group and 48.3 (0.7-61.3) in the placebo group

158 1230 confirmed HER2-positive patients in the lapatinib group and in 208 (17%) of 1260 in the placebo

159 ase-free survival events had occurred in the lapatinib group versus 264 (17%) in the placebo group (h

160 ere enrolled: 154 (34%) were assigned to the lapatinib group, 149 (33%) to the trastuzumab group, and

161 -free survival was 78% (95% CI 70-84) in the lapatinib group, 76% (68-82) in the trastuzumab group, a

162 ts in the trastuzumab group, 35 [20%] in the lapatinib group, and 46 [27%] in the combination group;

163 in the trastuzumab group, seven (4%) in the lapatinib group, and one (<1%) in the combination group;

164 ated recently that the 4-anilinoquinazolines lapatinib (GW572016, 1) and canertinib (CI-1033) kill T.

165 Lapatinib had significant PFS benefit over control (haza

166 rastuzumab and the tyrosine kinase inhibitor lapatinib have complementary mechanisms of action and sy

167 nd small molecule kinase inhibitors, such as lapatinib, have been developed, rapid identification and

168 In cells that grew in the presence of lapatinib, HER2 autophosphorylation was undetectable, wh

169 pecific inhibitor BYL719 in combination with lapatinib impaired mammary tumor growth and PI3K signali

170 vent leading to permanent discontinuation of lapatinib in affected patients.

171 ith a HER2-enriched profile may benefit from lapatinib in combination with endocrine therapy.

172 Treatment with trastuzumab or lapatinib in combination with taxane chemotherapy (pacli

173 was dependent on ERBB2; targeting ERBB2 with lapatinib in combination with the RAF inhibitor PLX4720

174 The combination of letrozole-lapatinib in early breast cancer was feasible, with expe

175 en PIK3CA mutation and response to letrozole-lapatinib in HR-positive/HER2-negative early breast canc

176 rge, randomized, placebo-controlled trial of lapatinib in human epidermal growth factor receptor 2-po

177 ) analysis in amorphous solid dispersions of lapatinib in hypromellose phthalate (HPMCP) and hypromel

178 mab, lapatinib, or combined trastuzumab plus lapatinib in patients with human epidermal growth factor

179 ation review suggested marginal benefit with lapatinib in terms of disease-free survival.

180 (n = 42) showed no significant benefit with lapatinib in terms of PFS and overall survival ( P > .05

181 ting a number of genes caused sensitivity to lapatinib in this context.

182 atic breast cancer to receive trastuzumab or lapatinib, in combination with a taxane, from January 17

183 gher sHER2 predicts greater PFS benefit with lapatinib independent of tHER2 status.

184 Mechanistically, the synergy was based on a lapatinib induced inhibition of the multidrug-resistance

185 Lapatinib-induced FOXO transcription factors, normally t

186 carriage as a predictor of increased risk of lapatinib-induced liver injury and implicate an immune p

187 itors of PI3K/AKT prevented trastuzumab- and lapatinib-induced stimulation of MLK3 activity.

188 o gain insight into the structural basis for lapatinib interaction with TbLBPKs, we constructed three

189 The strategy of extracting lapatinib intermolecular drug interactions from the tota

190 Lapatinib is an EGFR/HER2 kinase inhibitor suppressing s

191 e of its modest efficacy, the HER2 inhibitor lapatinib is currently used predominantly in combination

192 eracted in an additive fashion to facilitate lapatinib lethality.

193 was conducted using a 3+3 design with plasma lapatinib level monitoring.

194 Lapatinib may be an effective alternative therapy to cet

195 ngs shed new light on mechanisms involved in lapatinib-mediated autophagy in Her2-expressing breast c

196 Thus lapatinib might be an option for women with HER2-positiv

197 i-ERBB2 Mabs, suggesting that the effects of lapatinib might mainly be through ERBB1.

198 r the HPMC-E3 rich preparations showing that lapatinib molecules do not cluster in the same way as ob

199 trastuzumab continued to show superiority to lapatinib monotherapy in PFS (hazard ratio [HR], 0.74; 9

200 CTC-directed therapeutics and suggests that lapatinib monotherapy is not having any demonstrable cli

201 vival (PFS) and clinical benefit rate versus lapatinib monotherapy, offering a chemotherapy-free opti

202 omen were enrolled and 3147 were assigned to lapatinib (n=1571) or placebo (n=1576).

203 (84%) who were randomly assigned to receive lapatinib or control in the trials EGF30001, EGF30008, a

204 man primary DCIS was reduced further by DAPT/lapatinib or DAPT/gefitinib regardless of ErbB2 receptor

205 tch inhibitor, DAPT, and ErbB1/2 inhibitors, lapatinib or gefitinib.

206 risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in

207 is largely blocked in cells pretreated with lapatinib or pertuzumab.

208 to trastuzumab alone and in combination with lapatinib or pertuzumab.

209 cycles) were randomly assigned one to one to lapatinib or placebo after completion of first-line/init

210 nical and biologic effects of letrozole plus lapatinib or placebo as neoadjuvant therapy in hormone r

211 tive patients received either trastuzumab or lapatinib or the combination plus anthracycline-taxane c

212 PIM1 restored MAPK or PI3K activation after lapatinib or trastuzumab treatment, but rather inactivat

213 cy of pazopanib plus vorinostat, everolimus, lapatinib or trastuzumab, and MEK inhibitor in patients

214 during or after treatment with trastuzumab, lapatinib, or both, were eligible.

215 during or after treatment with trastuzumab, lapatinib, or both.

216 thracycline in combination with trastuzumab, lapatinib, or combined trastuzumab plus lapatinib in pat

217 ve early-stage breast cancer to trastuzumab, lapatinib, or the combination for 6 weeks followed by th

218 ve early-stage breast cancer to trastuzumab, lapatinib, or the combination for 6 weeks followed by th

219 f 3 neoadjuvant treatment arms: trastuzumab, lapatinib, or the combination for 6 weeks followed by th

220 lihood of pCR after neoadjuvant trastuzumab, lapatinib, or their combination when given with chemothe

221 ting agents have gained regulatory approval: lapatinib, pertuzumab, and trastuzumab-emtansine.

222 r sHER2 values still independently predicted lapatinib PFS benefit (HR per 10-ng/mL increase in sHER2

223 Lapatinib PFS benefit is independently predicted by high

224 9.6 months with T-DM1 versus 6.4 months with lapatinib plus capecitabine (hazard ratio for progressio

225 and overall survival with less toxicity than lapatinib plus capecitabine in patients with HER2-positi

226 grade 3 or 4 adverse events were higher with lapatinib plus capecitabine than with T-DM1 (57% vs. 41%

227 and overall survival with less toxicity than lapatinib plus capecitabine.

228 -plantar erythrodysesthesia were higher with lapatinib plus capecitabine.

229 d with trastuzumab and a taxane, to T-DM1 or lapatinib plus capecitabine.

230 was higher with T-DM1 (43.6%, vs. 30.8% with lapatinib plus capecitabine; P<0.001); results for all a

231 ore frequent with lapatinib (27 [17.5%]) and lapatinib plus trastuzumab (15 [9.9%]) than with trastuz

232 her with lapatinib (36 patients [23.4%]) and lapatinib plus trastuzumab (32 [21.1%]) than with trastu

233 nts randomly assigned with strata (n = 291), lapatinib plus trastuzumab continued to show superiority

234 the trastuzumab group, and 152 (33%) to the lapatinib plus trastuzumab group.

235 Lapatinib plus trastuzumab improves outcomes relative to

236 Phase III EGF104900 data demonstrated that lapatinib plus trastuzumab significantly improved progre

237 In addition, the drug combination (i.e. lapatinib plus YM155) decreased neuroblastoma tumor size

238 In contrast, lapatinib radiosensitized RAD51KD and RT112 cells but no

239 ncogene, the ErbB2 tyrosine kinase inhibitor lapatinib reduced the activation of ErbB3 and Akt as wel

240 Using a femtosecond pulsed laser, lapatinib release from a nanoshell-based human serum alb

241 reased Src kinase activity is a mechanism of lapatinib resistance and support the combination of HER2

242 oproteome changes in an established model of lapatinib resistance to systematically investigate initi

243 estigated and in the case of NIBP (TRAPPC9), lapatinib resistance was found to be mediated through NF

244 or verteporfin, eliminated modulus-dependent lapatinib resistance.

245 sts new biomarkers and treatment options for lapatinib-resistant cancers.

246 an innovative therapeutic agent for TZ- and lapatinib-resistant ErbB-2-positive BC and GC.

247 Lapatinib-resistant ERBB2-amplified breast cancer cell l

248 ta/PDGF and ErbB pathways with imatinib plus lapatinib, respectively, not only prevented myofibroblas

249 Five candidates, including lapatinib, SB-202190, RO-316233, GW786460X and indirubin

250 Using the lapatinib-sensitive breast cancer cell lines BT474 and S

251 ally blocked PI3K-Akt signaling and restored lapatinib sensitivity.

252 d capecitabine and 241 [49%] of 495 received lapatinib (separately or in combination) after study dru

253 the receptor tyrosine kinase (RTK) inhibitor lapatinib significantly improves survival, yet tumor res

254 Upon lapatinib stimulation, activated FOXO3a displaces FOXM1

255 antly alter the Km for ATP or sensitivity to lapatinib, suggesting that, unlike EGFR lung cancer muta

256 , we constructed three-dimensional models of lapatinib*TbLBPK complexes, which confirmed that TbLBPKs

257 ER3 signaling can be inactivated by doses of lapatinib that fully inactivate the HER2 kinase.

258 egative/HER2-enriched disease benefited from lapatinib therapy (median PFS, 6.49 vs 2.60 months; prog

259 Neoadjuvant lapatinib therapy in HER2(+) breast tumors lead to a sig

260 reast carcinoma cells that do not succumb to lapatinib, this Her1/2 inhibitor disrupts the cell surfa

261 An investigational arm of paclitaxel plus lapatinib (TL) was closed early.

262 lls with obatoclax enhanced the lethality of lapatinib to a greater extent than concomitant treatment

263 Adding lapatinib to fulvestrant does not improve PFS or OS in a

264 ts in outcome by the addition of maintenance lapatinib to standard of care.

265 inhibitor suppressing c-Myc synergizes with lapatinib to suppress cancer growth in vivo, partly by r

266 he pCR rates were 16%, 24.3%, and 17.4% with lapatinib, trastuzumab, and the combination, respectivel

267 logic complete response (pCR) to neoadjuvant lapatinib, trastuzumab, and their combination.

268 cells with acquired or innate resistance to lapatinib, trastuzumab, neratinib, and afatinib, all of

269 of mice with BT474 xenografts compared with lapatinib/trastuzumab (P = 0.0012).

270 The combination of LJM716/lapatinib/trastuzumab significantly improved survival of

271 In lapatinib-treated patients, the overall risk for Nationa

272 In lapatinib-treated patients, there was a significant diff

273 Lapatinib treatment of BT474 or SKBR3 cells resulted in

274 esses the induction of HER3 that accompanies lapatinib treatment of HER2-amplified cancers and synerg

275 Combined DAPT/lapatinib treatment was more effective at reducing acini

276 owed no evidence of plateau during 1 year of lapatinib treatment.

277 patients experiencing hepatotoxicity during lapatinib treatment.

278 by PRKACA and PIM1, and sensitized cells to lapatinib treatment.

279 bition against several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by ax

280 ne, in 3-week cycles, stratified by previous lapatinib use.

281 nts with advanced breast cancer treated with lapatinib using data from three randomized trials.

282 eraction) < .001) and by positive tHER2 (HR [lapatinib v nonlapatinib]: tHER2 positive, 0.638 v tHER2

283 dian PFS was 4.7 months for fulvestrant plus lapatinib versus 3.8 months for fulvestrant plus placebo

284 ykerb Evaluation After Chemotherapy [TEACH]: Lapatinib Versus Placebo In Women With Early-Stage Breas

285 Lapatinib was administered on days 1 through 5 of repeat

286 For HER2-positive tumors, lapatinib was associated with longer median PFS (5.9 v 3

287 The antiproliferative effect of lapatinib was inversely proportional to the elastic modu

288 st cancer drugs, docetaxel and HER2-targeted lapatinib, were delivered to MDA-MB-231 and SKBR3 (overe

289 ll survival, including in cells resistant to lapatinib, where cytotoxicity could be restored.

290 We examined whether lapatinib which binds both HER2 and EGFR could induce de

291 nhibitor; the MAPK signal inhibitor PD98059; lapatinib, which inhibits both the epidermal growth fact

292 ation in combination with either imatinib or lapatinib, which inhibits NHEJ and cell survival assesse

293 reated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total path

294 ilities, we combined the EGFR/HER2 inhibitor lapatinib with a novel small molecule, CBL0137, which in

295 Coadministration of lapatinib with obatoclax caused synergistic cell killing

296 Coadministration of lapatinib with obatoclax elicited autophagic cell death

297 ctivity after combining both trastuzumab and lapatinib with the anti-VEGFR2 antibody.

298 luate the therapeutic potential of combining lapatinib with the HDACi panobinostat in colorectal canc

299 were screened, in the presence or absence of lapatinib, with an RNA interference library targeting 36

300 CALGB 40302 sought to determine whether lapatinib would improve progression-free survival (PFS)